The ability to induce cell death by various members of the TNF family has been pursued by oncologists for almost 20 years. Originally, TNF itself was used to treat solid tumors and eventually was found to be applicable to the local treatment of melanoma by whole limb perfusion (Lejeune et al. (1998) Curr Opin Immunol 10:573)) Most recently, activation of TNF receptors by ligands or anti-receptor antibodies has sparked clinical interest. Activation of the Fas receptor, for example, has shown considerable promise, although it may be limited by liver toxicity. Activation of TRAILR1 or TRAILR2 by the TRAIL ligand, another member of the TNF family, has been reported to transduce an apoptotic signal to TRAIL-sensitive cancer cells (Griffith et al., J. Immunol. 162:2597, 1999; and Degli-Esposti et al., Immunity, 7:813-820, 1997). Activation of LT-β-R, yet another member of the TNF family, by soluble ligands or agonistic antireceptor monoclonal antibodies has also been shown to induce the death of certain carcinomas (Lawerence et al., (2001) Nat Med 7:383, Ichikawa et al., (2001) Nat Med 7:954). Treatment with agonist TNF activating agents would thus be useful for treating or reducing the advancement, severity or effects of neoplasia in subjects (e.g., humans).